Purpose. To clarify the role of perforin-and Fas ligand (L)-mediated cytotoxicity pathogenesis of viral myocarditis. Materials and methods. Forty balb/c mice were randomly divided into experimental group (n = 20) and ...Purpose. To clarify the role of perforin-and Fas ligand (L)-mediated cytotoxicity pathogenesis of viral myocarditis. Materials and methods. Forty balb/c mice were randomly divided into experimental group (n = 20) and control group (n = 20), and inoculated intraperitoneally with coxsackievirus B3(CVB3) and Eagle’s solu- tion without CVB3, respectively. The mice were sacrificed and their hearts were removed at day 7 post-in- oculation. Expression of perform and FasL were detected with immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization. Results. (1)Perform-and FasL-positiye cells were demonstrated in experimental murine hearts by im- munohistochemistry, however, no cells were discovered in control murine hearts; (2) The examination of RT-PCR showed the positive ratios of perform and FasL mRNA in myocardium were significantly higher in experimental group (100% and 100 % ) than that in control group (20% and 30 %, P<0.05); (3)Positive signals of perform and FasL mRNA were found in myocardium of all the experimental mice by in situ hybridization, but nothing was detected in control group. Conclusion. Perform and FasL can be expressed in infiltrating cells in murine myocardium with acute myocarditis caused by CVB3, suggesting perform and FasL might play an important role in pathogenesis of viral myocarditis.展开更多
The effect of verapamil on Ca2+ influx across the myocardial plasma membrane and coxsackie virus B3 ( CVB3)-RNA replication in cultured neonatal rat heart cells infected with CVB3 was investigated. It was found that t...The effect of verapamil on Ca2+ influx across the myocardial plasma membrane and coxsackie virus B3 ( CVB3)-RNA replication in cultured neonatal rat heart cells infected with CVB3 was investigated. It was found that the Ca2+ influx could be inhibited significantly (P<O. 01) by verapamil (1 μmol/L) after infection of heart cells for 48h. However, when the cultured heart cells infected with CVB3 and treated with verapamil (Iμmol/L and 10 nmo/L) at the same time for 48h, the amounts of CVB3-RNA in myocytes were significantly higher than that in infected control group (P<O. 05). These phenomena suggest that the increase of Ca2+ influx of cultured heart cells infected with CVB3 could be inhibited by some calcium antagonists, e. g. verapamil at the early stage. On the other hand, verapamil might accelerate viral replication in myocardium. Thus, although verapamil could be beneficial for decreasing the secondary Ca2+ damages and improve the myocardial electric activity, it isn’t a sensible choice for therapy in early stage of virus infection with cardiac symptoms.展开更多
文摘Purpose. To clarify the role of perforin-and Fas ligand (L)-mediated cytotoxicity pathogenesis of viral myocarditis. Materials and methods. Forty balb/c mice were randomly divided into experimental group (n = 20) and control group (n = 20), and inoculated intraperitoneally with coxsackievirus B3(CVB3) and Eagle’s solu- tion without CVB3, respectively. The mice were sacrificed and their hearts were removed at day 7 post-in- oculation. Expression of perform and FasL were detected with immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization. Results. (1)Perform-and FasL-positiye cells were demonstrated in experimental murine hearts by im- munohistochemistry, however, no cells were discovered in control murine hearts; (2) The examination of RT-PCR showed the positive ratios of perform and FasL mRNA in myocardium were significantly higher in experimental group (100% and 100 % ) than that in control group (20% and 30 %, P<0.05); (3)Positive signals of perform and FasL mRNA were found in myocardium of all the experimental mice by in situ hybridization, but nothing was detected in control group. Conclusion. Perform and FasL can be expressed in infiltrating cells in murine myocardium with acute myocarditis caused by CVB3, suggesting perform and FasL might play an important role in pathogenesis of viral myocarditis.
文摘The effect of verapamil on Ca2+ influx across the myocardial plasma membrane and coxsackie virus B3 ( CVB3)-RNA replication in cultured neonatal rat heart cells infected with CVB3 was investigated. It was found that the Ca2+ influx could be inhibited significantly (P<O. 01) by verapamil (1 μmol/L) after infection of heart cells for 48h. However, when the cultured heart cells infected with CVB3 and treated with verapamil (Iμmol/L and 10 nmo/L) at the same time for 48h, the amounts of CVB3-RNA in myocytes were significantly higher than that in infected control group (P<O. 05). These phenomena suggest that the increase of Ca2+ influx of cultured heart cells infected with CVB3 could be inhibited by some calcium antagonists, e. g. verapamil at the early stage. On the other hand, verapamil might accelerate viral replication in myocardium. Thus, although verapamil could be beneficial for decreasing the secondary Ca2+ damages and improve the myocardial electric activity, it isn’t a sensible choice for therapy in early stage of virus infection with cardiac symptoms.
